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ERK and FRS2alpha phosphorylation induced by FGF-21 in Klotho expressing cells. Klotho expressing HEK 293EBNA cells were serum starved for 16hr and then stimulated with hFGF-23-His, FGF-23-Fc (Prod. No. AG-40A-0109), mCD137-Fc (Fc control) and FGF
ERK and FRS2alpha phosphorylation induced by FGF-21 in Klotho expressing cells. Klotho expressing HEK 293EBNA cells were serum starved for 16hr and then stimulated with hFGF-23-His, FGF-23-Fc (Prod. No. AG-40A-0109), mCD137-Fc (Fc control) and FGF
ERK and FRS2alpha phosphorylation induced by FGF-21 in Klotho expressing cells. Klotho expressing HEK 293EBNA cells were serum starved for 16hr and then stimulated with hFGF-23-His, FGF-23-Fc (Prod. No. AG-40A-0109), mCD137-Fc (Fc control) and FGF

FGF-23 (human):Fc (human) (rec.)

Research Use Only
AG-40A-0109
AdipoGen Life Sciences
Protein IDQ9GZV9
Product group Proteins / Signaling Molecules
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Overview

  • Supplier
    AdipoGen Life Sciences
  • Product Name
    FGF-23 (human):Fc (human) (rec.)
  • Delivery Days Customer
    10
  • Certification
    Research Use Only
  • Concentration
    1 mg/ml
  • Estimated Purity
    >90%
  • Formulation
    Liquid
  • Protein IDQ9GZV9
  • Protein Name
    Fibroblast growth factor 23
  • Scientific Description
    FGF-23 (Fibroblast growth factor 23) is a regulator of phosphate homeostasis. It upregulates EGR1 expression in the presence of KLBy. Acts directly on the parathyroid to decrease PTH secretion. Regulates the vitamin-D metabolism. Negatively regulates osteoblast differentiation and matrix mineralization. Defects in FGF-23 are the cause of autosomal dominant hypophosphataemic rickets (ADHR) and of hyperphosphatemic familial tumoral calcinosis (HFTC). - Protein. Signal peptide and human FGF-23 (aa 1-251) are fused at the C-terminus to the Fc portion of human IgG1. Source: HEK 293 cells. Endotoxin content: <0.1EU/microg purified protein (LAL test; Lonza). Liquid. 0.2microm-filtered solution in PBS. Purity: >90% (SDS-PAGE). FGF-23 (Fibroblast growth factor 23) is a regulator of phosphate homeostasis. It upregulates EGR1 expression in the presence of KLBy. Acts directly on the parathyroid to decrease PTH secretion. Regulates the vitamin-D metabolism. Negatively regulates osteoblast differentiation and matrix mineralization. Defects in FGF-23 are the cause of autosomal dominant hypophosphataemic rickets (ADHR) and of hyperphosphatemic familial tumoral calcinosis (HFTC).
  • Storage Instruction
    -20°C,2°C to 8°C
  • UNSPSC
    12352202